Responsiveness of a modified version of the postural assessment scale for stroke patients and longitudinal change in postural control after stroke- Postural Stroke Study in Gothenburg (POSTGOT) -

Abstract Background Responsiveness data certify that a change in a measurement output represents a real change, not a measurement error or biological variability. The objective was to evaluate the responsiveness of the modified version of the Postural Assessment Scale for Stroke Patients (SwePASS) in patients with a first event of stroke. An additional aim was to estimate the change in postural control during the first 12 months after stroke onset. Methods The SwePASS assessments were conducted during the first week and 3, 6 and 12 months after stroke in 90 patients. Svensson’s method, Relative Position (RP), Relative Concentration (RC) and Relative Rank Variance (RV), were used to estimate the scale’s responsiveness and the patients’ change in postural control over time. Results From the first week to 3 months after stroke, the patients improved in terms of postural control with 2 to 12 times larger systematic changes in Relative Position (RP), for which 9 items and the total score showed a significant responsiveness to change when compared to the intrarater reliability measurement error of the SwePASS reported in a previous study. When SwePASS was used to assess change in postural control between the first week and 3 months, 74% of the patients received higher scores while 10% received lower scores, RP 0.31 (95% CI 0.219-0.402). The corresponding figures between 3 and 6 and between 6 and 12 months were 37% and 16%, RP 0.09 (95% CI 0.030-0.152), and 18% and 26%, RP −0.07 (95% CI −0.134- (−0.010)), respectively. Conclusions The SwePASS is responsive to change. Postural control evaluated using the SwePASS showed an improvement during the first 6 months after stroke. The measurement property, in the form of responsiveness, shows that the SwePASS scoring method can be considered for use in rehabilitation when assessing postural control in patients after stroke, especially during the first 3 months.</p

Comparing Employment Trajectories before and after First Imprisonment in Four Nordic Countries

Employment plays a crucial role in the re-entry process and in reducing recidivism among offenders released from prison. But at the same time, imprisonment is generally regarded as harmful to post-release employment prospects. Little is known, however, about whether or not offenders’ employment trajectories before and after imprisonment are similar across countries. As a first step towards filling this gap in research, this paper provides evidence on employment trajectories before and after imprisonment in four Nordic welfare states: Denmark, Finland, Norway and Sweden. Using data gathered from administrative records on incarcerated offenders, the analysis focuses on individuals imprisoned for the first time and who served a prison sentence less than one year in length. Results show that although employment trajectories develop in mostly similar ways before and after imprisonment across these countries, important differences exist.Peer reviewe

Novel mutation in TNPO3 causes congenital limb-girdle myopathy with slow progression

Objective We report a second family with autosomal dominant transportinopathy presenting with congenital or early-onset myopathy and slow progression, causing proximal and less pronounced distal muscle weakness. Methods Patients had clinical examinations, muscle MRI, EMG, and muscle biopsy studies. The MYOcap gene panel was used to identify the gene defect in the family. Muscle biopsies were used for histopathologic and protein expression studies, and TNPO3 constructs were used to study the effect of the mutations in transfected cells. Results We identified a novel heterozygous mutation, c.2757delC, in the last part of the transportin-3 (TNPO3) gene in the affected family members. The mutation causes an almost identical frameshift affecting the stop codon and elongating the C-term protein product of the TNPO3 transcript, as was previously reported in the first large Spanish-Italian LGMD1F kindred. TNPO3 protein was increased in the patient muscle and accumulated in the subsarcolemmal and perinuclear areas. At least one of the cargo proteins, the splicing factor SRRM2 was normally located in the nucleus. Transiently transfected mutant TNPO3 constructs failed to localize to cytoplasmic annulate lamellae pore complexes in cells. Conclusions We report the clinical, molecular genetic, and histopathologic features of the second transportinopathy family. The variability of the clinical phenotype together with histopathologic findings suggests that several molecular pathways may be involved in the disease pathomechanism, such as nucleocytoplasmic shuttling, protein aggregation, and defective protein turnover.Peer reviewe

Differences in hip bone mineral density may explain the hip fracture pattern in osteoarthritic hips

Introduction In patients with osteoarthritis of the hip (OAH), trochanteric fractures are much more common than femoral neck fractures. One reason may be altered bone composition in the proximal femurs. OAH often leads to a fixed external rotation of the hip, leading to difficulties in positioning during DXA measurements. We compared BMD in OAH-affected legs and healthy legs

July 2017 ENCALS statement on edaravone

Peer reviewe

Использование принципа клиентоориентированности при формировании стратегии развития предприятий

Материалы межвуз. науч. конф. студентов, магистрантов и аспирантов, Гомель, 15 мая 2008 г

The Clinical and Pathological Spectrum of Idiopathic Inflammatory Myopathies : Implications for pathogenesis, classification and diagnosis

Background: Idiopathic inflammatory myopathies (IIM) constitute a heterogeneous group of diseases with severe consequences for the life of affected patients. Dermatomyositis, polymyositis and inclusion body myositis (IBM) are the classical representatives of this group. The treatments given today often have limited effects, and are taken at the cost of side effects. Major obstacles in the search for more effective treatments are; (1) an incomplete understanding of the disease mechanisms, (2) difficulties to delineate homogeneous disease groups for clinical studies and (3) the sometimes challenging task to diagnose these diseases. Aims: We addressed a number of “loose ends” in the areas of pathogenesis, classification and diagnosis; mechanisms of muscle fiber degeneration in IIM, with a focus of programmed cell death (apoptosis) and invasion of muscle  fibers by inflammatory cells (partial invasion); protecting and mediating factors present in muscle; the association of other diseases with IIM, in particular celiac disease ; the evaluation of two classification systems and laboratory methods for increased diagnostic performance. The studies: We included 106 patients, diagnosed at the Neuromuscular unit in Linköping, Sweden, with pathological muscle findings consistent with IIM. The incidence in the county of Östergötland (during 5 years) was 7.3 per million/year (3 patients each year). Of 88 patients with confirmed IIM 4 (4.5 %) had celiac disease, 33 (38%) had an associated systemic inflammatory disease and 5 (5.7 %) had a malignancy. Ninety-nine patients were included for a comparison of two classification systems using criteria of the European Neuromuscle Centre (Amato/ENMC), and the widely used Bohan and Peter classification, both with the addition of IBM according to Griggs et al. Using the Amato/ENMC criteria the most prevalent diagnostic group after IBM (30%) was nonspecific myositis (23%), followed by polymyositis (20%) and dermatomyositis 17%). A substantial number of patients meeting Bohan and Peter (or Griggs) criteria were excluded by Amato/ENMC criteria, most (21/23) due to lack of detectable muscle weakness. Extended muscle sectioning increased the sensitivity of a muscle biopsy by 15 % and the specificity by 22%, and showed an overlap between disease groups. Muscle biopsies from patients with IIM and controls were used to investigate pathological findings considered specific for disease groups, and for the presence of programmed cell death (apoptosis) and disease protecting and mediating factors in muscle. The presence of apoptotic muscle fiber nuclei was detected in muscle with partial invasion (however not in the invaded fibers) in the presence of granzyme B and CD8+ cytotoxic T cells. The major apoptosis inhibiting protein Bcl-2 was shown to be constitutionally expressed in healthy muscle but weakened in IIM. Conclusion: We present apoptosis as a possible disease mechanism in parallel with partial invasion of fibers. Furthermore, partial invasion may not be a suitable distinguishing feature in the pathogenesis, or for classification and diagnosis of IIM. We also introduce the anti-apoptotic Bcl-2 as a possible relevant muscle fiber protecting factor. A more extensive pathological work-up improves classification and diagnosis of IIM. The proposed Amato/ENMC creates a substantial portion of patients with non-specific or unclassified myositis. Associated diseases are common in IIM, and also include celiac disease